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Mitochondrial Free Radical Production and Caloric Restriction: Implications in Vertebrate Longevity and Aging

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Book cover Oxidative Stress in Aging

Part of the book series: Aging Medicine ((AGME))

Summary

In this chapter, studies focusing on the relationship between oxidative stress and aging in different vertebrate species and in calorie-restricted animals are reviewed. Endogenous antioxidants inversely correlate with species maximum longevity, and experiments modifying their levels can increase survival and mean life span but not maximum life span. Evidence shows that long-lived vertebrates consistently have low mitochondrial free radical generation rates and also a low fatty acid unsaturation of cellular membranes, two crucial factors determining their aging rate. Oxidative damage to mitochondrial DNA is also lower in long-lived vertebrates than in short-lived vertebrates. Conversely, caloric restriction, the best described experimental manipulation that consistently increases mean and maximum life span, also decreases mitochondrial reactive oxygen species (ROS) generation and oxidative damage to mitochondrial DNA. Recent data suggest that the decrease in mitochondrial ROS generation would be due to protein restriction rather than calories, pointing out a key role for dietary methionine. Longevity would be achieved in part due to a low endogenous oxidative damage generation rate, but also due to a macromolecular composition highly resistant to oxidative modification, as it is the case for lipids and proteins.

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Acknowledgements

Our results described in this review were supported by grant BFU2005-02584 from the Ministry of Science and Education and from CAM/UCM groups (910521) (to G.B.).

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López-Torres, M., Barja, G. (2008). Mitochondrial Free Radical Production and Caloric Restriction: Implications in Vertebrate Longevity and Aging. In: Miwa, S., Beckman, K.B., Muller, F.L. (eds) Oxidative Stress in Aging. Aging Medicine. Humana Press. https://doi.org/10.1007/978-1-59745-420-9_9

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